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Metastasis 76 LiH.LiC
Although oxidative stress, mitochondrial damage, and cell death involved in the pathogenesis of APAP hepatotoxicity have been reported [25], accumulating studies on the pathogenesis of APAP hepatotoxicity indicate that subsequent inflammatory responses of the immune system critically determine the severity and outcome of disease [26, 27]
Cyanidin ameliorates endotoxin-induced myocardial toxicity by modulating inflammation and oxidative stress through mitochondria and other factors
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GAS6/AXL signaling pathway The GAS6/AXL axis, a key member of the TAM (TYRO3, AXL, MERTK) receptor tyrosine kinase family, is frequently overactivated in solid tumors and is strongly associated with therapy resistance
